title: [Clinical and experimental study of traumatic optic nerve damage].
abstract: BACKGROUND
  Traumatic optic nerve lesions (TONL) range from temporary affection of vision to avulsion of the optic nerve; often they are associated with more complex injuries. Usually Tonl are not regarded as an emergency. Up to now, we lack knowledge on the dependency of strength and duration of optic nerve lesions and the point of no return for afferent disorders of the visual pathway.
  
  
  METHODS
  We performed a prospective study on 50 patients with severe midface and skullbase fractures in order to find characteristic ophthalmological, computer tomographic und electrophysiological findings as indicators of TONL, independent of patient cooperation. We used an animal model (Wistar rats; n = 117) to study calibrated optic nerve lesions and the resulting neurodegeneration in the retinal ganglion cell (RGC) layer quantitatively.
  
  
  RESULTS
  The electrophysiological investigation of the visual system (flash VEP/ERG) proved to be highly specific (0.97) and sensitive (1.0) for detecting TONL (n = 18). In the rat model, we could demonstrate a linear relationship between total neuron number reduction and strength and duration of calibrated optic nerve lesion.
  
  
  CONCLUSIONS
  Experimental results indicate that optic nerve decompression is useful only within the first hours after TONL to reduce secondary optic nerve lesion. Indication for optic nerve decompression requires early detection of TONL, which is made possible by the combination of flash VEP/ERG.
authors.affiliation: Klinik und Poliklinik für Mund-, Kiefer- und Gesichtschirurgie, Albert-Ludwigs-Universität Freiburg.
authors.forename: N C
authors.initials: NC
authors.lastname: Gellrich
authors.forename: M M
authors.initials: MM
authors.lastname: Gellrich
authors.forename: M
authors.initials: M
authors.lastname: Zerfowski
authors.forename: H
authors.initials: H
authors.lastname: Eufinger
authors.forename: U T
authors.initials: UT
authors.lastname: Eysel
mesh_terms: D000818:Animals; D002452:Cell Count; D004596:Electroretinography; D005074:Evoked Potentials, Visual / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D009410:Nerve Degeneration / Q000473:pathology / Q000503:physiopathology; D009900:Optic Nerve / Q000473:pathology / Q000503:physiopathology; D020221:Optic Nerve Injuries; D011446:Prospective Studies; D051381:Rats; D017208:Rats, Wistar; D012165:Retinal Ganglion Cells / Q000473:pathology / Q000502:physiology; D019291:Skull Base / Q000293:injuries; D012887:Skull Fractures / Q000473:pathology / Q000503:physiopathology*; D014795:Visual Pathways / Q000293:injuries / Q000473:pathology / Q000503:physiopathology
vernacular_title: Klinische und experimentelle Untersuchung zur traumatischen Sehnervenschädigung.